Research has identified that long term use of medications for treatment of obesity in patients has resulted in many problems. The two most significant problems encountered by patients using medications to assist in weight loss, assuming the absence of irreversible side effects from the medications, are that:
The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.
In the past long term treatment, defined as treatment longer than 3 months to many years, with medications, has raised safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.
A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem.
In the past obesity or weight management procedures, as noted in U.S. Pat. No. 5,795,895, implement a single dosing schedule of SSRI medication for a patient. A single dosing schedule of SSRI medication is not optimal for a desired level of weight loss performance. Individuals frequently fail to lose a desired amount of weight when alternative doses of medication are unavailable.
Second, patients receiving treatment for weight loss through the use of medication frequently experience complications such as a cessation of performance of the medication due to a “nutritional deficiency”. Frequently it is difficult to predict which patients are likely to experience unacceptable performance of weight loss medication due to “nutritional deficiencies” associated with calorie deficit's.
It is also problematic to predict the outcome of medication treatment upon individuals receiving Norepinephrine medications such as Phentermine and/or Diethylpropion. These medications have unique chemical properties making the outcome of treatment of patients uncertain. In addition not all medications function to assist in weight loss. In the past SSRI (selective Serotonin Reuptake Inhibitor) medications which have been used in weight loss include Fluoxetine Hydrochloride (Prozac), Sertraline (Zoloft), Fluvoxamine Maleate (Luvox), and Trazodone Hydrochloride (Desyrel).
The treatment programs for obesity as known also teach away from the use of alternative dosing procedures to effectuate weight loss. Specifically U.S. Pat. No. 5,795,895 teaches that an SSRI medication never needs to be raised to improve the anorexiant effect of weight loss and that the SSRI medication level administered to a patient may be raised to assist in the treatment of coexisting conditions such as depression.
It is therefore desirable to have a weight loss treatment program for a patient which provides for an effective therapeutic range of available medication to enhance desired weight loss. It is also desirable to provide a weight loss program which minimizes the percent of individuals who do not initially respond to the medication treatment regime or who cease to continue to receive the beneficial effects of the weight loss program following the initiation of the medication treatment due to nutritional deficiencies. These and other problems are solved by the disclosed Comprehensive Pharmacologic Therapy For Treatment Of Obesity.
A problem has been known in the past where drugs which work on norepinephrine stop working after a period of time when used in treating patients for weight loss. As stated in Wurtman et. al in U.S. Pat. No. 4,885,312.
Indirect-acting sympathomimetic amines (such as Phentermine) function by releasing stored norepinephrine from sympathetic nerve endings. The major problem with their use is that after a few doses, they often stop functioning, i.e., tachyphylaxis sets in. Tachyphylaxis is known to be associated with partial depletion of the norepinephrine in the nerve endings, leading to the supposition that there are releasable and non-releasable pools of norepinephrine and that when the drugs cease functioning, it is because the releasable pools have been severely depleted. The chemical pathway involved is:

Dopa, doparnuie, norepinephrine, and epinephrine are known as “catecholamines”. Chemically the enzyme “Tyrosine Hydroxylase” limits the rate of formation of catecholamines. Another problem as known is to identify a way to increase the amounts of Tyrosine Hydroxylase or it's activity in a patient receiving treatment for obesity. No procedure is known which uses a dietary precursor approach to increase amounts of Tyrosine Hydroxylase and it's activity in a patient receiving treatment for obesity. No procedure is known to increase catecholamine levels in a patient by providing the precursor needed for the formation of Tyrosine Hydroxylase.
Catecholamine formation is regulated by a feed back loop involving norepinephrine and Tyrosine Hydroxylase. In this loop norepinephrine binds to each of the four legs of the Tyrosine Hydroxylase enzyme and through the mechanism of phosphorylation the norepinephrine deactivates Tyrosine Hydroxylase into a new chemical known as “phosphorylated Tyrosine Hydroxylase”. In the process the body begins to synthesis more Tyrosine Hydroxylase.
A complication in the treatment of patients for weight loss is that drugs which are given to increase the levels of intersynaptic norepinephrine lead to increased phosphorylation of Tyrosine Hydroxylase which, in turn, causes increased synthesis of Tyrosine Hydroxylase and depletion of critical precursors. The net effect of drugs which cause increased intersynaptic levels of norepinephrine for a patient is the depletion of precursors need in the synthesis of Tyrosine Hydroxylase leading to the “tachyphylaxis”. The provision to a patient of the precursor Tyrosine with co-factors vitamin C, calcium, and vitamin B6 will not prevent or reverse the tachyphylaxis induced by drugs which cause increased levels of intersynaptic norepinephrine.